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Biomedical subjects

Z Sheng

Publications and source records attributed to Z Sheng.

At least 91 records · Page 5Linked to original sources
PubMed1996

In vivo effects of tumor necrosis factor-alpha on incised wound and gunshot wound healing.

Recombinant tumor necrosis factor alpha (TNF-alpha) was applied to incised wounds (adult rats, n = 14) and gunshot wounds (dogs, n = 5). The accumulation of RNA and DNA in regenerative tissue, the wound disruption strength (WDS), and histology were examined. The results showed that a single dose of TNF-alpha in saline with highly purified bovine serum albumin increased the WDS and accumulation of RNA and DNA in regenerative tissue in incised wounds 3 days after surgery (p < 0.05). Also, TNF-alpha promoted the inflammatory reaction in the wounded area of gunshot wounds. Histology revealed increased capillary tube-like structures and collagen formation and fibroblast proliferation in both incised and gunshot wounds treated with TNF-alpha. The results indicated that locally applied TNF-alpha benefited the incised and gunshot wound healing. These mitogenic and inflammatory effects of TNF-alpha may be the synergistic effects with other growth factors such as platelet-derived growth factor (PDGF).

Animals↗
PubMed1996

Cardiotrophin-1 displays early expression in the murine heart tube and promotes cardiac myocyte survival.

We have recently isolated a novel cytokine, cardiotrophin-1 (CT-1), from an in vitro embryonic stem cell system of cardiogenesis that can activate embryonic markers in neonatal rat cardiac myocytes. CT-1 is a new member of the interleukin 6 (IL-6)/leukemia inhibitory factor (LIF) cytokines, which activate downstream signals via gp130-dependent pathways. To define the developmental pattern of expression of CT-1 during murine embryogenesis, we have developed antibodies directed against a CT-1 fusion protein. As assessed by immunolocalization, CT-1 is predominantly expressed in the early mouse embryonic heart tube (E8.5-10.5). In the heart, CT-1 is primarily expressed in myocardial cells, and not in endocardial cushion or outflow tract tissues. After E12.5, CT-1 expression is found in other tissues, including skeletal, liver and dorsal root ganglia. Given the effects of a related family member (ciliary neurotrophic factor, CNTF) on neuronal cell survival, we studied the ability of CT-1 to promote cardiac myocyte survival and proliferation in vitro. Both CT-1 and LIF, which share the same receptors, dramatically promote neonatal cardiac myocyte survival, while IL-6 and CNTF are without effect. A cell proliferation assay documents that CT-1 provokes an approximate 2-fold increase in embryonic cardiac myocyte proliferation. Thus, CT-1 may play an autocrine role during cardiac chamber growth and morphogenesis by promoting the survival and proliferation of immature myocytes, most likely via gp130-dependent signaling pathways.

Animals↗
PubMed1996

Research into analgesia by inhaling analgesic.

This article deals with analgesia by inhaling analgesic. According to Chinese medical theories, TCM analgesics were chosen from the literature and folk prescriptions screened and proved by analgesic tests on animals. A reasonable prescription was made up and the drug inhaled. Its analgesic effect was superior to that of dolantin injection (3 mg/kg body weight, intraperitoneal injection). Clinical trials showed its analgesic effect in 3-10 minutes and it lasted for more than 2 hours in over 70% of the cases for a total effective rate of 94.6%. The drug is absorbed quickly and acts directly on the nerve center. Its use is not addictive.

Administration, Inhalation↗
PubMed1996

[Effect of escharectomy during burn shock stage on bacterial and endotoxic translocation from the gut].

120 SPF rats (Wistar) were randomly divided into 3 groups (1) simple skin grafting group (Group A). (2) Escharectomy during burn shock group (Group B). (3) Routine escharectomy group (Group C) Full-thickness burn of 30% TBSA was produced in Group B and Group C. One hour after scald intravenous fluid replacement was instituted. First stage escharectomy has been performed 24 hours after burn and 5 days postburn. The results demonstrated that the contents of both plasma LPS and TNF in Group B were significantly lower as compared with these in Group C. Our data indicated escharectomy during burn shock would effectively eliminate the effects of the endotoxemia. Endotoxin play an important role in the bacterial and endotoxic translocation.

Animals↗
PubMed1995

The functional role of the domains of troponin-C investigated with thrombin fragments of troponin-C reconstituted into skinned muscle fibers.

Proteolysis of rabbit fast skeletal troponin-C (RSTnC) with thrombin produces four separate fragments containing the following Ca2+-binding site(s): TH1 (residues 1-120) sites I-III; TH2 (121-159) site IV; TH3 (1-100) sites I and II; and TH4 (101-120) site III. We studied the ability of these fragments to restore the steady state isometric force in TnC-depleted skinned skeletal muscle fibers. Interestingly, we found that all investigated fragments of RSTnC possessed some of the properties of native RSTnC, but none of them could fully regulate contraction in the fibers like intact RSTnC. TH1 was the most effective in the force restoration (65%) whereas the smaller fragments developed about 50% (TH3 and TH4) or 20% (TH2) of the initial force of unextracted fibers. Additionally, much higher concentrations of TH2, TH3, and TH4 compared to RSTnC OR TH1 were necessary for force development suggesting a decreased affinity of these fragments to their binding site(s) in the fibers. Like intact RSTnC, TH1 was able to interact with the fibers in a Ca(2+)-independent (Mg(2+)-dependent) manner, indicating that at a minimum, Ca(2+)-binding site III is required for this type of binding. The initial binding of the other fragments to the TnC-depleted fibers occurred only in the presence of Ca2+. TH2 and TH4 appeared to bind to two different binding sites in the fibers. The binding to one of the sites caused partial force restoration. This binding of TH2 and TH4 was abolished when Ca2+ was removed. TH2 and TH4 binding to the second site required Ca2+ initially but was maintained in the presence of Mg2+. This interaction of TH2 and TH4 partially blocked the rebinding of RSTnC to the fibers. The latter results suggest that site III and IV in these small fragments, when removed from the constraints of the parent protein, may assume conformations that allow them to function, to a certain extent, like both the regulatory sites (I and II) and the Ca(2+)-Mg2+ sites(III and IV) of TnC.

Animals↗
PubMed1995

Independent regulation of sterol regulatory element-binding proteins 1 and 2 in hamster liver.

Two sterol regulatory element-binding proteins (SREBPs, designated SREBP-1 and SREBP-2), each approximately 1150 amino acids in length, are attached to membranes of the endoplasmic reticulum and nuclear envelope in human and hamster tissue culture cells. In the absence of sterols, soluble fragments of approximately 470 amino acids are released from both proteins by proteolytic cleavage. The soluble fragments enter the nucleus, where they bind to sterol regulatory elements in the promoters of genes encoding the low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl CoA synthase, thereby activating transcription. Proteolytic processing of both SREBPs is blocked coordinately by sterol overloading and enhanced coordinately when sterols are depleted by treatment with an inhibitor of cholesterol synthesis. In contrast to these findings in cultured cells, the current data show that SREBP-1 and -2 are not coordinately regulated in hamster liver. In untreated animals the soluble fragment of SREBP-1, but not of SREBP-2, was detected by immunoblotting of a liver nuclear extract. Depletion of sterols by treatment with a bile acid-binding resin (colestipol) and a cholesterol synthesis inhibitor (mevinolin) led to a marked increase in the nuclear form of SREBP-2 and a reciprocal decline in the nuclear form of SREBP-1. These findings suggest that SREBP-1 is responsible for basal transcription of the low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl CoA synthase genes in hamster liver and that SREBP-2 is responsible for the increased transcription that follows sterol depletion with a bile acid-binding resin and a cholesterol synthesis inhibitor.

Animals↗
PubMed1995

A direct regulatory role for troponin T and a dual role for troponin C in the Ca2+ regulation of muscle contraction.

Troponin (Tn), containing three subunits: Ca2+ binding (TnC), inhibitory (TnI), and tropomyosin binding (TnT), plays a crucial role in the Ca2+ regulation of vertebrate striated muscle contraction. These three subunits function by interacting with each other and with the other thin filament proteins. Previous studies suggested that the primary role of TnT is to anchor the TnI.TnC complex to the thin filament, primarily through its interactions with TnI and tropomyosin. We propose here a new role for TnT. Our results indicate that, when TnT is combined with the TnI.TnC complex, there is an activation of actomyosin ATPase that is Ca(2+)-dependent. To determine whether the latter results from a direct effect of TnC on TnT or indirectly from an effect of TnC on TnI which is transmitted to TnT, we prepared a deletion mutant (deletion of residues 1-57) of TnI, TnId57 (Sheng et al. (1992) J. Biol. Chem. 267, 25407-25413), which interacts with TnC but not TnT. Both wild type (TnI.TnC.TnT) and mutant (TnId57.TnC.TnT) Tn complexes demonstrated equivalent activity in the Ca2+ regulation of actomyosin-S1 ATPase activity. Similarly, both TnI and TnId57 could equally reconstitute TnI-depleted skinned muscle fibers. Therefore, since TnId57 does not interact with TnT, these results suggest that TnT reconstitutes native Ca2+ sensitivity via direct interaction with TnC. Thus Ca2+ binding to TnC would have a dual role: 1) release of the ATPase inhibition by TnI and 2) activation of the ATPase through interaction with TnT.

Animals↗
PubMed1995

C-type inactivation of a voltage-gated K+ channel occurs by a cooperative mechanism.

The lymphocyte voltage-gated K+ channel, Kv1.3, inactivates by a C-type process. We have elucidated the molecular basis for this process using a kinetic analysis of wild-type and mutant (A413V) Kv1.3 homo- and heteromultimeric currents in a mammalian lymphoid expression system. The medians of the measured inactivation time constants for wild-type and A413V homotetrameric currents are 204 and 4 ms, respectively. Co-expression of these subunits produces heteromultimeric channels manifesting inactivation kinetics intermediate between those of wild-type and A413V homomultimers. We have considered several models in which each subunit acts either independently or cooperatively to produce the observed inactivation kinetics. The cooperative model gives excellent fits to the data for any heteromultimeric composition of subunits, clearly distinguishing it from the independent models. In the cooperative model, the difference in free energy between the open and inactivated states of the channel is invariant with subunit composition and equals approximately 1.5 kcal/mol. Each subunit contributes equally to the activation free energy for transitions between open and inactivated states, with an A413V subunit decreasing the free energy barrier for inactivation (and for recovery from inactivation) by approximately 0.6 kcal/mol. Our results are consistent with a physical model in which the outer mouth of the channel constricts during C-type inactivation (G. Yellen, D. Sodickson, T. Chen, and M.E. Jurman, 1994, Biophys. J. 66:1068-1075).

Animals↗
PubMed1995

Evidence of serological cross-reactivities with human immunodeficiency virus types 1 and 2 and human T-lymphotropic virus types I and II in sera of pregnant women in Ibadan, Nigeria.

BACKGROUND: Our previous studies have indicated that the human immunodeficiency virus (HIV) and human T-lymphotropic virus (HTLV) groups of retroviruses are endemic among various populations in Nigeria. These viruses are antigenically distinct and antibodies to HIV and HTLV do not cross-react, so we studied the prevalence of HIV-1, HIV-2, HTLV-I and HTLV-II antibodies in sera of pregnant women attending an antenatal clinic in Ibadan, Nigeria. METHODS: In all, 364 sera were screened using three different enzyme immunoassays, including those that distinguished HIV-1 antibodies from HIV-2, and HTLV-I antibodies from HTLV-II. All repeatedly reactive sera were confirmed by Western blots and synthetic peptide assays for the respective viruses. RESULTS: Overall, 71 sera (19.5%) had antibodies to HIV, HTLV or both groups of retroviruses. Most (95.8%) of the reactive samples were from women 20-29 years old. Two of five sera from individuals < 20 years old reacted for HIV antibodies while one serum from a 40 year old woman was reactive for HTLV-I antibodies. Of the 71 reactive sera, 29 (8%) had antibodies to HIV (HIV-1 = 14, HIV-2 = 9, HIV-1/2 = 6) and 42 samples (11.5%) showed antibodies to HTLV (HTLV-I = 20, HTLV-II = 14, HTLV-I/II = 8). Seven of 71 seropositive samples (9.8%) reacted for both HIV and HTLV antibodies in various combinations, including one serum that showed antibody reactivities to all four retroviruses (i.e. HIV-1, HIV-2, HTLV-I and HTLV-II). CONCLUSIONS: The high prevalence of antibodies to subtypes of the two entirely distinct retrovirus groups in young women has important implications for defining epidemiological patterns of diseases associated with co-infections with two or more retroviruses.

Adolescent↗
PubMed1995

Acidic fibroblast growth factor reduces rat skeletal muscle damage caused by ischemia and reperfusion.

Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad-spectrum mitogenic and non-mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aFGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatase (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of extra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future.

Adenosine Triphosphatases↗
PubMed1995

[Protective effects of vitamin E on impaired neutrophil phagocytic function in patients with severe burn].

The protective effects of vitamin E on impaired neutrophil phagocytic function were observed in 22 patients with severe burn. The results showed that lowering of SOD values, elevation of MDA values significantly elevated and impairment of neutrophil phagocytic function were all more marked in the patients who did not receive vitamin E than that of vitamin E treated groups and the healthy control. It was also found that there was a significant inverse correlation between MDA values of blood plasma and neutrophil phagocyte rate and phagocyte index in the patients without vitamin E treatment. The results suggested that in severely burned patients the use of free radical scavenger and antioxidant could protect the neutrophil function to certain extent. The optimal dosage of vitamin E will be further assessed.

Adolescent↗
PubMed1995

[Multiple organ injury after delayed fluid resuscitation in severely scalded rats: role of oxygen free radicals].

Sixty gnotobiotic rats with 5 strains of bacteria in intestine were randomized to 4 groups: (1) Sham injury group (controls, n = 6). (2) Early fluid resuscitation (EFR) group (n = 24), receiving fluid resuscitation (Parkland formula) immediately after scald (40% TBSA, third degree). (3) Delayed fluid resuscitation (DFR) group (n = 24) receiving resuscitation 6 hours later after scald. (4) Treatment group (n = 12) receiving DFR and the therapy of VitC and VitE. At 8, 24, 48 and 72 hours after injury, the animals (n = 6, at each point) were sacrificed and the content of oxygen free radicals (OFR), SOD,GSHPx and MDA in the heart, liver, kidney and lung were determined. Morphological Changes of organs, PaO2, PaCO2 and the content of serum CPK, LDH, GPT, GOT, BUN and Cr were also examined. Both EFR and DFR groups demonstrated elevated content of OFR and MDA and reduced content of SOD and GSHPx in their organs. Morphological and serological changes were also observed. All these changes were more obvious in DFR group than in EFR group. After the treatment of VitC and VitE, the changes were ameliorated. Our results suggested that DFR induced the production of OFR, resulting in lipid peroxidation and that OFR injury might be one of the main factors in the pathogenesis of multiple organ injury after DFR.

Animals↗
PubMed1995

Extensive wound excision in shock stage in patients with major burns.

To stop excessive plasma loss, alleviate noxious effects of devitalized tissues on the body and shorten the hospitalization time, we performed extensive escharectomy during the shock period in extensively burned patients. Group A consisted of 21 patients aged 9-45 years (26.1 +/- 7.9 years), with a mean total burn area of 63.2% +/- 18.1% TBSA, and full-thickness injury involving 35.9% +/- 19.6% TBSA. The first escharectomy was done at 24.1 +/- 13.9 hours postburn, and excision area averaged 32.3% +/- 6.7% TBSA (24%-46%). In 15 of them, Swan-Ganz catheter was introduced to monitor the hemodynamic changes. It was found that RAP, PAP, PAWP, ABP, HR, CO and CI were all stable during and after the operation. Group B consisted of 29 patients aged 11-50 years (30.4 +/- 11.7 years), in whom escharectomy was begun 4-5 days postburn. The mean healing time of the patients in group A was 33.1 days, shorter than that of group B patients (40.1 days). The duration of hemoconcentration was shorter in group A. The amount of blood transfusion was almost 700 ml less in group A during the first two weeks. Less antibiotics were used with fewer visceral complications in group A. We believe that escharectomy during the burn shock stage is feasible.

Adolescent↗
PubMed1995

[Escharectomy during burn shock stage contributed to controlling or alleviating infectious complication].

Among 29 patients with extensive burn, 14 received escharectomy during the shock period, and the other 15 after 96 hrs. LPS and TNF were determined before and after escharectomy 3, 7, 14 and 21 PBD. Incidence of sepsis and subeschar bacterial count were analyzed. Clinical conditions were compared. The results showed that escharectomy during burn shock stage significantly reduced infectious complications in extensively burned patients. We believe that as long as general condition of the patient allowed, early removal of eschar was beneficial in reducing the threat of sepsis.

Adult↗
PubMed1995

Ischemia and reperfusion reduce the endogenous basic fibroblast growth factor (bF GF) in rat skeletal muscles.

Polyclonal antibodies directed against human recombinant basic fibroblast growth factor (bFGF) were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. bFGF immunoreactivity was found mainly in the extracellular matrix, primarily in the endomysium, including the heparin-containing basal lamina and also in the capillary basal membrane of both normal and wounded muscles, however the signal intensity was much stronger in normal muscles. After 4-hour ischemia, about 40% of skeletal muscle fibers lost their bFGF immunoreactivity. Muscles which experienced 4-hour ischemia and 24 reperfusion had only a weaker bFGF immunoreactivity. The pathological results supported the concept of destroyed cell connection and fiber necrosis in ischemia and reperfused muscles. The mechanisms involved in this reduced concentration of bFGF in wounded muscles included oxygen radical activation, inflammatory response and reduced secretion of endogenous bFGF. These results were only partially compatible with the established mitogenic role of this protein and suggested that a reduction of endogenous FGF may partly contribute to a delay in wound healing.

Animals↗
PubMed1995

[Clinical effects of naloxone on hemorrhagic shock].

In order to study the clinical effects of naloxone on hemorrhagic shock, 21 patients with moderate hemorrhagic shock were randomly divided into two groups. The naloxone group (NLX group) was infused normal saline (200ml) and naloxone (0.02mg/kg) via central vein while the control group was infused normal saline (200ml) only. Mean arterial pressure (MAP), central vein pressure (CVP), cardiac output (CO), cardiac index (CI), peripheral vascular resistance (PVR), levels of lactic acid in both artery and vein, and levels of catecholamine in artery were measured before and after the administration of naloxone or normal saline. The results showed that naloxone significantly increased blood level of catecholamine and MAP (P < 0.01), the effects sustained for more than 15 minutes with an increased PVR (P < 0.05). After infustion of normal saline, blood level of lactic acid in artery and vein decreased slightly (P > 0.05), yet comparatively lower in artery. On the contrary, after administration of naloxone, the blood level of lactic acid markedly decreased in both artery and vein (P < 0.01), but higher in artery. It is suggested that naloxone improve tissue oxygen supply temporarily with enhancement of tissue lactic acid metabolism.

Aged↗
PubMed1994

Inhibition of hepatic chylomicron remnant uptake by gene transfer of a receptor antagonist.

The low density lipoprotein receptor-related protein (LRP) has been proposed to mediate in concert with the LDL receptor (LDLR) the uptake of dietary lipoproteins into the hepatocytes. This hypothesis was tested by transient inactivation of LRP in vivo. Receptor-associated protein (RAP), a dominant negative regulator of LRP function, was transferred by an adenoviral vector to the livers of mice lacking LDLR (LDLR-/-). The inactivation of LRP by RAP was associated with a marked accumulation of chylomicron remnants in LDLR-/- mice and to a lesser degree in normal mice, suggesting that both LDLR and LRP are involved in remnant clearance.

Adenoviridae↗